RESUMO
OBJECTIVE: This study aims to investigate rat hippocampal cartilage glycoprotein-39 (YKL-40) expression levels following status epilepticus (SE), and the potential mechanism of YKL-40 in SE-induced neuronal injury. METHODS: Seventy-two healthy adult male Sprague-Dawley rats were randomly assigned into two groups: control and SE groups. A lithium chloride-pilocarpine SE model was established, and the control group was injected with sodium chloride. The hippocampus was assessed at three, six, 12, 24 and 72h after SE. YKL-40 protein was detected via immunohistochemistry (n=6). Cellular YKL-40/neuronal nuclei antigen (NeuN) expression levels were determined with double immunofluorescence. YKL-40 mRNA was detected via quantitative real-time polymerase chain reaction (qRT-PCR, n=6). RESULTS: YKL-40 immunoreactivity was poor and was mainly localized to the cytoplasm within hippocampal CA3/CA4 neurons with limited immunoreactivity in the nucleus in the control group. Following SE, YKL-40 immunoreactivity exhibited a diffused distribution throughout the cytoplasm in neurons and increased distribution in the nucleus. CA3 and CA4 YKL-40 protein expression significantly increased at six hours post-SE (P<0.05), peaked at 12h (P<0.01), and decreased at 24h (P<0.05) and 72h (P<0.05) in the SE group, compared with the control group. Double-label immunofluorescence of YKL-40/NeuN exhibited a hippocampal CA3/CA4 neuron location. Furthermore, SE induced a significant increase inYKL-40 mRNA at six, 24, or 72h (P<0.05); which peaked at 12h (P<0.01). CONCLUSIONS: YKL-40 was expressed in neurons, and elevated rat hippocampal YKL-40 expression levels may be involved in the pathogenesis of injury following SE.